Research
Print page Print page
Switch language
Rigshospitalet - a part of Copenhagen University Hospital
Published

Fibroblast Growth Factor (FGF) 23 Regulates the Plasma Levels of Parathyroid Hormone In Vivo Through the FGF Receptor in Normocalcemia, But Not in Hypocalcemia

Research output: Contribution to journalJournal articleResearchpeer-review

  1. Multiple Fractures and Impaired Bone Fracture Healing in a Patient with Pycnodysostosis and Hypophosphatasia

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Bone Mass Development in Childhood and Its Association with Physical Activity and Vitamin D Levels. The CHAMPS-Study DK

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Hyperkalemia is Associated with Increased 30-Day Mortality in Hip Fracture Patients

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Nye hormoner relateret til calcium- og fosfathomøostasen ved nyresygdom

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Effect of inhibition of CBP-coactivated β-catenin-mediated Wnt signalling in uremic rats with vascular calcifications

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Pathophysiology and reversibility of uremic vasculopathy

    Research output: Book/ReportPh.D. thesisResearch

View graph of relations

The calcium and phosphate homeostasis is regulated by a complex interplay between parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and calcitriol. Experimental studies have demonstrated an inhibitory effect of FG23 on PTH production and secretion; the physiological role of this regulation is however not well understood. Surprisingly, in uremia, concomitantly elevated FGF23 and PTH levels are observed. The parathyroid gland rapidly loses its responsiveness to extracellular calcium in vitro and a functional parathyroid cell line has currently not been established. Therefore, the aim of the present investigation was to study the impact of FGF23 on the Ca2+/PTH relationship in vivo under conditions of normocalcemia and hypocalcemia. Wistar rats were allocated to treatment with intravenous recombinant FGF23 and inhibition of the FGF receptor in the setting of normocalcemia and acute hypocalcemia. We demonstrated that FGF23 rapidly inhibited PTH secretion and that this effect was completely blocked by inhibition of the FGF receptor. Furthermore, inhibition of the FGF receptor by itself significantly increased PTH levels, indicating that FGF23 has a suppressive tonus on the parathyroid gland's PTH secretion. In acute hypocalcemia, there was no effect of either recombinant FGF23 or FGF receptor inhibition on the physiological response to the low ionized calcium levels. In conclusion, FGF23 has an inhibitory tonus on PTH secretion in normocalcemia and signals through the FGF receptor. In acute hypocalcemia, when increased PTH secretion is needed to restore the calcium homeostasis, this inhibitory effect of FGF23 is abolished.

Original languageEnglish
JournalCalcified Tissue International
Volume102
Issue number1
Pages (from-to)85-92
Number of pages8
ISSN0171-967X
DOIs
Publication statusPublished - 2018

    Research areas

  • Journal Article

ID: 52424539